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The hand foot, and mouth disease (HFMI)) epidemic has become a serious public health problem worldwide with a high economic and health burden. In addition, the prevalence of (HFMI) varies greatly between cities. Therefore, this paper aims to reveal high-risk cities for HFMD and associated meteorological and air pollution factors in Guangdong Province during 2014-2018. Data on the incidence of HFMD mid meteorological and air pollution. factors were obtained from the Guangdong Provincial Center for Disease Control and Prevention and Guangdong Meteorological Service. Three different grey incidence analysis (GIA) were used, namely Deng's grey incidence analysis, absolute degree of GIA, and second synthetic degree of GIA. Additionally, GMC (1,1) model was used to predict the trend of HFMD in 2019-2028. According to the second synthetic degree of GIA, the top three cities most affected by HFMD are Zhuhai, Guangzhou, and Foshan. However, the prediction model .found that the incidence of HFMD in Guangdong Province will generally decline in the next 10 years, indicating that the prevention and control measures are still relatively in place. Deng's grey incidence analysis found that CO, %O2, PM2.5, PM10), and wind scale are closely related to the incidence of HFMD. It is recommended to closely monitor weather change and urban air quality and take protective measures against HFMD in advance. The results of this study hare substantial implications for the control of HFMD. [ABSTRACT FROM AUTHOR]

Enteroviruses can frequently target the human central nervous system to induce a variety of neurological diseases. Although en-teroviruses are highly cytolytic, emerging evidence has shown that these viruses can establish persistent infections both in vivo and in vitro. Here, we investigated the susceptibility of three human brain cell lines, CCF-STTG1, T98G, and SK-N-SH, to infection with three entero virus serotypes: coxsackievirus B3 (CVB3), entero virus 71, and coxsackievirus A9. Persistent infection was observed in CVB3-infected CCF-STTG1 cells, as evidenced by prolonged detection of infectious virions, viral RNA, and viral antigens. Of note, infected CCF-STTG1 cells expressed the nonfunctional canonical viral receptors coxsackievirus-adenovirus receptor and decay-accelerating factor, while removal of cell surface chondroitin sulfate from CCF-STTG1 cells inhibited the replication of CVB3, suggesting that receptor usage was one of the major limiting factors in C VB3 persistence. In addition, CVB3 curtailed the induction of beta interferon in infected CCF-STTG1 cells, which likely contributed to the initiation of persistence. Furthermore, proinflammatory chemokines and cytokines, such as vascular cell adhesion molecule 1, interleukin-8 (IL-8), and IL-6, were upregulated in CVB3-infected CCF-STTG1 cells and human progenitor-derived astrocytes. Our data together demonstrate the potential of CCF-STTG1 cells to be a novel cell model for studying C VB3-central nervous system interactions, providing the basis toward a better understanding of CVB3-induced chronic neuropathogenesis. [ABSTRACT FROM AUTHOR]

Enteroviruses can frequently target the human central nervous system to induce a variety of neurological diseases. Although enteroviruses are highly cytolytic, emerging evidence has shown that these viruses can establish persistent infections both in vivo and in vitro. Here, we investigated the susceptibility of three human brain cell lines, CCF-STTG1, T98G, and SK-N-SH, to infection with three enterovirus serotypes: coxsackievirus B3 (CVB3), enterovirus 71, and coxsackievirus A9. Persistent infection was observed in CVB3-infected CCF-STTG1 cells, as evidenced by prolonged detection of infectious virions, viral RNA, and viral antigens. Of note, infected CCF-STTG1 cells expressed the nonfunctional canonical viral receptors coxsackievirus-adenovirus receptor and decay-accelerating factor, while removal of cell surface chondroitin sulfate from CCF-STTG1 cells inhibited the replication of CVB3, suggesting that receptor usage was one of the major limiting factors in CVB3 persistence. In addition, CVB3 curtailed the induction of beta interferon in infected CCF-STTG1 cells, which likely contributed to the initiation of persistence. Furthermore, proinflammatory chemokines and cytokines, such as vascular cell adhesion molecule 1, interleukin-8 (IL-8), and IL-6, were upregulated in CVB3-infected CCF-STTG1 cells and human progenitor-derived astrocytes. Our data together demonstrate the potential of CCF-STTG1 cells to be a novel cell model for studying CVB3-central nervous system interactions, providing the basis toward a better understanding of CVB3-induced chronic neuropathogenesis. [ABSTRACT FROM AUTHOR]

Human Enterovirus 71 (EV71) and Coxsackievirus B3 (CVB3) have high risks for morbidity and mortality. A virus quantitation immunoassay has been proposed by employing two colored quantum dots (QDs), antibodies of the virus, and graphene oxide (GO). The QDs are streptavidin-conjugated quantum dots (SA-QDs), and the antibodies are biotinylated antibodies. Biotinylated EV71 antibody (Ab1) was associated with 525 nm green colored SA-QDs via biotin-streptavidin interaction forming QDs-Ab1, whereas biotinylated CVB3 antibody (Ab2) was associated with 605 nm red colored SA-QDs via biotin-streptavidin interaction forming QDs-Ab2. GO was an excellent quencher to the fluorescence of both QDs-Ab1 and QDs-Ab2. The targets of EV71 and CVB3 can break up the complex of QDs-Ab and GO, recovering the fluorescence of QDs-Ab1 and QDs-Ab2, respectively. Using these two different colored QDs-Ab fluorescence recovery intensities upon the addition of targets EV71 and CVB3, the two enteroviruses can be simultaneously quantitatively determined with a single excitation light. The detection limits of EV71 and CVB3 are 0.42 and 0.39 ng mL-1 based on 3 times signal-to-noise ratio, respectively. More importantly, this strategy can be further used as a universal method for any protein or virus determination by changing the conjugated antibodies in disease early diagnosis, which can provide a fast and promising clinical approach for virus differentiation and determination. In a word, a simple, fast, sensitive, and highly selective assay for EV71 and CVB3 has been developed. It could be applied in clinical sample analysis with a satisfactory result. It was notable that the sensor could not only achieve rapid and precise quantitative determination of protein/virus by fluorescent intensity but also could be applied in semiquantitative protein/virus determination by digital visualization. [ABSTRACT FROM AUTHOR]